Newer Concepts Regarding Physiologic Benefits of Exercise Training

A longstanding and attractive hypothesis is the concept that exercise training can reverse or retard the progression of atherosclerosis. The observation that regression of atherosclerosis occurred in animal studies dating back to the 1950s continues to stimulate interest in the effects of exercise on the coronary vasculature in humans. While this idea was largely rejected during the 1970s and 1980s, several notable studies were performed during the 1990s indicating that exercise training, when combined with multidisciplinary risk management, can improve myocardial perfusion.33-35 This has been demonstrated indirectly using nuclear imaging33 and directly by angiography.34,35 Because most of these studies involved multidisciplinary risk reduction (e.g. diet, smoking cessation, stress management, and pharmacologic management of risk factors, including statin therapy) in addition to exercise training, it is not possible to determine the independent effects of exercise training.

There is also debate regarding the mechanism by which the apparent improvement in myocardial perfusion might occur following training. It is generally considered unlikely that changes in coronary blood flow during exercise in animals would apply to humans. Three mechanisms could potentially explain an improvement in perfusion after training: (1) direct regression of atherosclerotic lesions; (2) formation of collateral vessels; or (3) a change in the dynamics of epicardial flow via flow-mediated or endogenous stimuli of the vessel. While there has been evidence of small but significant improvements in lumen diameter after intensive exercise and risk reduction programs in patients with CAD, no evidence exists that collateral vessel formation occurs after training in humans. Interestingly, although changes in lumen diameter following these intervention programs are quite small, they are associated with considerable reductions in hospital admissions for cardiac reasons.35 This suggests that patients in the intervention groups may achieve greater plaque stabil ity, without large changes in the coronary artery lumen.

In terms of the third mechanism, that is, changes in epicardial flow dynamics after training, a significant amount of recent research has demonstrated that training improves endothelial dysfunction, thus permitting enhanced peripheral and coronary blood flow in response to exercise. This represents a paradigm shift in the pathophysiology of CAD. The last decade has brought an awareness that the luminal diameter of epi-cardial vessels changes rapidly in response to mechanical (flow-related) and endogenous or pharmacological stimuli. Hambrecht et al.36 studied the effects of exercise training in patients with reduced ventricular function and reported that leg blood flow during acetylcholine infusion was enhanced compared to controls. The improvement after training was attributed to an increase in endothelium-dependent vasodilation with an increase in basal nitric oxide formation. In a subsequent study, these investigators demonstrated an improvement in endothelium-dependent vasodilation in epicardial vessels as well as resistance vessels in patients with CAD. After 4 weeks of exercise training, there was a 29% increase in coronary artery flow reserve in comparison to the non-exercise control group.37

These findings have been confirmed by other groups,38-40 and suggest an important role of endothelial dysfunction contributing to inadequate blood flow in patients with cardiovascular disease. Exercise training appears to have a profound effect on the vasodilatory properties of the vasculature. Further exploration into the effects of exercise training on the dynamic behavior of the endothelium is an important target area for future research in both patients with and without existing cardiovascular disease.

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